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Swine Atrophic Rhinitis: a Brief Review

Introduction

Atrophic rhinitis is an infectious bacterial disease described in the
early nineteenth century (Franque, 1830 - Germany). Thus, after
nearly two centuries of existence, its infectious aetiology is precisely
recognised a century later (Ratke, 1938 - Carlstrom, 1940) and there
is still clinical evidence on pig farms around the world. It has occurred
to a greater or lesser degree throughout this time and has been
significantly prevalent in this first decade of the 21st century.

The first thing I would like to point out is that two sets of well-defined
clinical symptoms are encompassed, at the same time, within this
infectious disease. They are:

Progressive Atrophic Rhinitis (PAR) caused by toxigenic type
D Pasteurella multocida as its primary agent either alone or
together with other infectious agents, the most characteristic
of which is Bordetella bronchiseptica.

Regressive or Non-progressive Atrophic Rhinitis (RAR), caused
by toxigenic Bordetella bronchiseptica. This concept was
coined by Pederson and Nielsen in 1983.

Both bacteria spread easily among the swine population, especially
when control measures implemented are insufficient to eliminate
them within the carriers existing on the farm.

The pigs themselves are the main transmitters of Bordetella bronchiseptica
(breeders, piglets, fattening pigs and replacement gilts), and
Pasteurella multocida is also able to spread to other animals such
as rats, cats, dogs, birds, chickens, sheep, goats, cattle, horses,
and even to humans (zoonoses). Without a doubt, the ability to
persist and transmission of both bacteria on farms is very high.

The characteristic lesion caused by both bacteria is bone hypoplasia
of nasal turbinates, of which pigs have two on each side: two ventral
and two dorsal, so a total of four. The severity of infection is determined
by the intensity of the damage in each of the four turbinates
(conchae) and the nasal septum that can lead to a more or less
alarming clinical atrophic rhinitis, which is linked to a more or less
pronounced lateral or facial torsion, marked tearing, and even nasal
haemorrhages. From what we have previously mentioned, the severity
of clinical cases is higher in cases of progressive atrophic rhinitis
caused initially by toxigenic Pasteurella multocida.

Another common factor in both clinical aspects of atrophic rhinitis
(PAR and RAR) is the considerable loss of growth with the added
factor of individual variability among pigs, which creates a great
heterogeneity in the fatteners, which is affected by a high percentage of smaller pigs and an increase in the number of days at the fattening
period and aggravated by the economic setback in the schedule of
charges at the abattoir and the associated treatment costs.

Thus atrophic rhinitis is a disease with significant economic impact on
our farms, which should lead us to take effective preventive measures
for control and containment. We should also take into account that
when we monitor farms that have demonstrated clinical symptoms,
their absence during certain periods does not guarantee that the
infection is absent from the breeders, so we may find clinical
relapses over time.

Aethiology

The primary origin of atrophic rhinitis is found in the toxigenic strains
of the bacteria, Pasteurella multocida and Bordetella bronchiseptica.
The conditions for growth and colonisation of both bacteria needed to
produce sufficient amounts of toxins are also determined by other
infectious agents, both viral and bacterial, which can damage the
nasal mucosa, as well as by multi-factorial environmental factors in
regard to adverse management and infrastructure. Each and every
one of these associated factors aggravates - to a greater or lesser
extent - the clinical presence of atrophic rhinitis on each farm.

Both Pasteurella multocida and Bordetella bronchiseptica are Gramnegative
bacteria of a similar size and aerobes with a coccobacilli
shape. Both bacteria are involved in upper and lower respiratory tract
disorders within the familiar Porcine Respiratory Disease Complex. We
also know that pigs with atrophic rhinitis are more susceptible to
respiratory complications.

We know the antigenic variation of both strains of Pasteurella multocida,
as well as Bordetella bronchiseptica that to a certain extent
determine which clinical features appear with the variable severity
stemming from them.

Within these extrinsic factors, which play a decisive influence in the
severity of atrophic rhinitis, we should point out the following:

Genetic factors: the role of heredity in the presentation of atrophic
rhinitis was suggested three decades ago; it was considered highly
variable according to lines and breeds of pigs (LW>LN). It was
thought there was a genetic predisposition between lines and strains
of toxigenic Pasteurella multocida that varied in susceptibility.
Nowadays we know that the risk is in the those genetics that are
carriers from the source farm which are multipliers of the toxigenic
bacteria Pasteurella multocida and/or Bordetella bronchiseptica.

Epidemiology

Bordetella bronchiseptica and Pasteurella multocida very effectively
colonise the mucosa of the respiratory tract after infection. These two
bacteria are highly prevalent in the swine population to a greater degree
than the clinical cases of atrophic rhinitis. With no problem, we could
refer to this as an “iceberg disease”, in which only a small part of the
health problem of our pigs is seen.

To correctly understand how clinical signs of atrophic rhinitis appear
more or less suddenly on a farm, which we believed to be disease free,
we should start with the idea that the infection and/or transmission of
these two bacteria take place in the early phases of a piglet's life. We
can isolate both bacteria in young piglets, especially at weaning. Bordetella
bronchiseptica can cause respiratory problems even in those
animals only a week old. It also easily colonises organs of the upper
respiratory apparatus.

Young replacement gilts are considered a key factor in the origin and/or
spread of atrophic rhinitis; they are active disseminators of both
bacteria. The presence of clinical signs in them is definitive, although
their absence does not exclude the fact that they may be carriers.
Hence, an exhaustive knowledge of the state of health in regard to
atrophic rhinitis, both progressive and regressive, of our replacement
animals (self-replacement or purchase of gilts from outside) is essential
in prevention and control programmes.

The infection cycle can be maintained on a farm over time by a very
small group of gilts and/or breeders that are carriers, in which the
bacteria are found in tonsils and intestines.

The entrance of positive replacement gilts into negative populations
will give rise to rapid spread of both progressive and regressive
atrophic rhinitis.

Breeder-carrier sows play a crucial role in the spread of infection within
a farm and transmit both bacteria during lactation to offspring and/or
piglets adopted by negative mothers. Similarly, the transmission of both
bacteria between breeders (replacement gilts, sows in production and
boars) is quite effective. At this point, we must consider the greater risk
of transmission on farms where the sows are housed in groups for at
least half of their production cycle and/or effective life. Neither
bacteria involved in atrophic rhinitis are transmitted via semen or
embryo transfer.

In addition to this vertical sow to piglet transmission in the early stages
of life, horizontal transmission by aerosol and faecal matter intake
between piglets when 5 to 8 weeks old is no less important. The
greatest elimination of both bacteria takes place within 2-3 weeks after
weaning, at the same time the starter phase begins. At this stage, the
infection may become endemic if the associated factors mentioned
above are favourable. The infection can be enhanced and spread rapidly
among the population of both sows and especially susceptible piglets,
and give rise to clinical symptoms of progressive or regressive atrophic
rhinitis, with the aggravating circumstance that it usually occurs at a later
age (fattening pigs), and this can lead to confusion at the time of first
contact and subsequent decisions. We can thereby ensure that infections in a pig’s early age are vital for the later development of the
disease.

Infections can last for months and are related to the degree and intensity
of the infection. Likewise, the degree of lesions and clinical signs are in
relation to whether the infection is early or late. The earlier it occurs, the
more serious it is.

Passive protection of piglets from naturally infected sows makes it possible
to reduce clinical incidence, but not their infection, which means the health
risk remains when the piglets are weaned and, of course, when they go on
to the growth and finishing phase.

Piglets from carrier mothers are infected from the second week of life
onwards (up to six weeks), whereas if these sows are well vaccinated
against Bordetella bronchiseptica and toxigenic Pasteurella multocida, the
infective potential moves to 14-18 weeks when the development of
progressive atrophic rhinitis is not feasible in intensive production with
sacrifice at 22-25 weeks.

Thus is not uncommon to see on unvaccinated farms the transfer of piglets
to fattening units that we believe are healthy, and when they reach 12-16
weeks of life, they show a severe progressive atrophic rhinitis. This is due
to high toxin production by Pasteurella multocida type D between 8-10
weeks of age, coinciding with entry into the fattening period.

Both Bordetella bronchiseptica and Pasteurella multocida are sensitive to
most disinfectants, as well as to low humidity and high temperatures (> 60 ºC
for less than 15 minutes). Infection pressure can be reduced by the
systemic depopulation between batches, washing with hot water and use
of disinfectants.

Pathogenesis

The different types of mucin produced in the nasal mucosa of pigs at
different ages tell us how both Bordetella bronchiseptica and Pasteurella
multocida colonise the mucosa. Bordetella bronchiseptica colonises and
adheres to the nasal mucosa where it preferentially attacks the ciliated
epithelial cells. It multiplies on the mucosal surface and produces toxins
that spread through the bone tissue of the turbinates causing degenerative,
proliferative and inflammatory changes in the nasal epithelium with
loss of cilia. There are variations between different strains according to
their toxigenic capacity. Of the four turbinates, the two ventral ones are
usually the most commonly affected. In severe cases, we see both the
dorsal and ventral turbinates affected. Susceptibility to this degree of
turbinate atrophy is reduced as the pig increases in age.

The modifications to the nasal epithelium caused by Bordetella bronchiseptica
are a great breeding ground for favouring the proliferation of
toxigenic type D Pasteurella multocida to produce epithelial hyperplasia,
atrophy of the turbinates, mesenteric cell proliferation, osteolysis, and
atrophy of nasal glands.

In controlled infections in piglets, it is feasible to have a partial or total
regeneration of the epithelium of the turbinates, so that the degree of
hypoplasia they undergo is related to a delay in their growth.

If we understand the importance of the nasal mucosa as a first line of
organic defence, the partial or total destruction of the turbinates in
cases of both progressive and regressive atrophic rhinitis leads to
greater susceptibility to respiratory complications and other opportunistic
infectious agents, whether from bacteria, viruses or parasites.

We can conclude that pathogenically the toxins of both bacteria are
different and produce alterations of nasal turbinates by different mechanisms, which give rise to the symptoms of both regressive and progressive
atrophic rhinitis.

Lesions and Clinical Signs

To gain a better understanding of clinical symptoms of atrophic rhinitis,
we should give a prior explanation of the clinical set of lesions it causes.
The gross lesions of both progressive and regressive atrophic rhinitis are
centred on the nasal cavity and adjacent structures. The main lesions we
can find are:

Atrophy of ventral and dorsal turbinates indistinctly or separately in
each individual with large variations in location and severity. In
severe cases, these structures may even disappear.

Atrophy and/or deviation of the nasal septum that may be symmetric
or asymmetric, with upward or sideways deviation of the snout.

Formation of mucopurulent exudates in the nasal cavity, which on
occasion may be accompanied by blood.

We may observe in clinical pictures of atrophic rhinitis secondary complications,
such as respiratory symptoms of the lower respiratory tract with
lesions from bronchopneumonia in apical and cardiac lobes of the lung.

The microscopic lesions that serve as a reference after the obvious
gross lesions are:

Fibrosis of osseous plates of nasal turbinates.

Inflammation of the laminates of the nasal mucosa with degenerative
processes.

The clinical symptoms of atrophic rhinitis may go unnoticed when
they first appear, and even more so in cases of regressive atrophic
rhinitis, in spite of the clinical evidence of the severe forms of
progressive atrophic rhinitis.

We can clearly identify the clinical display of progressive atrophic
rhinitis in fatteners, which is characterised by:

Lateral or frontal deviation of the snout.

Tearing and accumulated dirt in the corner of the eye due to
occlusion of the nasolacrimal duct. This does not always have a
linear direct relationship with atrophic rhinitis.

Sneezing with or without nasal exudates.

Epistaxis: blood in one or both of the nasal orifices.

Facial deformations: wrinkles on the snout and face.

Nasal hypertrophy on the sides of molars.

Evident delay of between 16-19 per cent in growth rates with reference to
the average rates quoted in the literature, which may exceed 30 per cent in
conventional pigs depending on severity.

Considerable increases of pigs with delayed growth, which leads to
loss of maximum value when slaughtered.

Symptoms of regressive atrophic rhinitis are no less frequent in which
clinical signs can be observed in young piglets (3-4 weeks of age or
earlier) that, despite being less apparent, do not have a lower economic
impact on production. In piglets affected by regressive atrophic rhinitis
we can find:

Frequent sneezing (we must differentiate coughing from sneezing).

Snorts with mucopurulent nasal exudates of varying degrees.

Less appetite than is normal for their physiology with delayed
growth (25-40 grams per day).

Diagnosis

Diagnosing progressive atrophic rhinitis a priori is easier than diagnosing
regressive atrophic rhinitis; it is based on clinical symptomatology.
However on farms where large amounts of antibiotics are used, these
external clinical symptoms may be hidden or masked.

In both cases, in addition to clinical diagnosis, we should ensure
and confirm the disease with the aid of the following diagnostic
techniques:

Post-mortem diagnosis based on a transversal cut of a pig's snout
at the level of the first to second upper premolar, and assessing the
degree of atrophy of each one of the four nasal turbinates. There are
various techniques for creating these lesions (0 to 5), but they vary
according to the instructor, in addition to not keeping a linear direct
relation with the severity of the forms of atrophic rhinitis. A minimum
number of snout samples are needed per batch so that the diagnosis
is significant (20 per cent).

Subsequent bacteriological exam using pulmonary wash on live pig
samples as well as those from the abattoir. It is much more precise
than a study based on nasal swabs or nasal exudates samples.
They should be shipped to the laboratory in phosphate saline
solution and refrigerated (4-8ºC). The seedings are done in blood
agar or MacConkey agar enriched with glucose 1 per cent. Analysis based
on tonsils and lungs is frequently used as a basis for diagnosis. The
determination of toxigenic strains is not easy using bacteriological
culture techniques, which means it is highly unlikely that we will
receive a definitive diagnosis.

Serology by detection of agglutinating antibodies in serum. The
information from this technique is less specific than that from
bacteriological culture in specific mediums. Serology does not
differentiate between antibodies of infected pigs or vaccinated pigs.
If they are not vaccinated, serology can help us in the primary
diagnosis of atrophic rhinitis.

We must take into account the following pathologies in regard to
differential diagnosis of atrophic rhinitis:

Infections by cytomegalovirus: rhinitis by inclusion bodies.

Influenza virus.

Aujeszky's disease.

Porcine Reproductive and Respiratory Syndrome Virus.

Poorly designed feeders and drinkers that determine maxillary
deformations.

Prevention and Control

Occasional and/or isolated measures of treatment or handling are not
sufficient for effectively resolving problems of either progressive or
regressive atrophic rhinitis.

Precise knowledge of the farm or productive structure is critical for
understanding the source of the problem while, at the same time, a
laboratory diagnosis is needed to support the epidemiological and
clinical diagnosis for the purpose of developing a programme of
measures for treatment, control and future prevention of both progressive
and regressive atrophic rhinitis.

To do so, we must consider all management and treatment measures,
the surroundings, genetics, nutrition and specific vaccination procedures
for preventing this infectious disease that has such a great economic
impact on production. The economic losses in each case will
justify the measures taken, because the return on investment for each
of them is considerable.

Basis for the principal objectives of these measures should be the
following points:

Reduce the prevalence - infection pressure of Bordetella bronchiseptica,
and Pasteurella multocida, both in the future breeder gilts,
as well as sows, piglets and fattening pigs.

Reduce the lesion scores in the nasal mucosa and turbinates
to neutralise the economic losses stemming from them on the
pigs’ production yields (growth, conversion).

Reduce the lesions for avoiding secondary bacterial infections
that aggravate the process and its symptoms.

Improve conditions of environmental comfort that facilitate
respiratory efficiency and the use of nutrients.

The first prevention measure against atrophic rhinitis would be
preventing the entrance to the firm of the Bordetella bronchiseptica
and toxigenic type D Pasteurella multocida bacteria, by means of
unapparent carriers such as future breeder gilts. The following steps
are needed to do so:

Know the health origin of the replacement gilts, along with the
treatment and vaccinations on the farm from which they come,
with the firm commitment of the parties to be free of both
progressive and regressive atrophic rhinitis.

Absence of apparent clinical signs upon entry and during the
strict nine-week quarantine phase.

Vaccination and re-vaccination with a 3-to-4-week interval during
the quarantine with an inactivated vaccine that contains both
bacteria (Bordetella bronchiseptica and toxigenic type D
Pasteurella multocida).

Once the gilts have entered the test farm, the use of a specific
vaccination schedule is prescribed with a vaccine mentioned which
includes:

Primary vaccination: two doses, at 8-7 and 4-3 weeks prior to
the indicated farrowing date. In acute cases, we can give a
blanket double vaccination to the entire breeder herd,
regardless of the state of reproduction in which they are found.

Revaccination in the following gestation with a single dose between
four and three weeks prior to the estimated farrowing date.

These highly effective vaccination measures, should, at all times, be
accompanied by the prescribed measures shown in practice to be
positive, listed below:

Strict depopulation practices: cleaning, washing, disinfection
and time empty between production batches of lactating sows,
piglets and fattening pigs. Washing will be even more effective
if done with hot water.

Reduce the density of animals in the same space.

Strict measures of biosecurity: absence of cats, dogs, birds,
rats; as well as contact with pigs with other susceptible production
animals such a sheep, goats, cattle or horses.

The additional combined use of therapeutic measures with vaccines
that prevent Bordetella bronchiseptica and toxigenic type D Pasteurella
multocida help us reduce the lesion severity and associated
symptoms, particularly the acute clinical cases, while simultaneously
improving production rates of infected pigs, both piglets and
fatteners.

The main antibiotics that have been shown to be sensitive to
Bordetella bronsicheptica and toxigenic Pasteurella multocida are:

It is important to choose the correct antibiotic, taking into account
the age, dosage rate, timing, withdrawal periods and costs per pig.
The combined use of therapeutics should always be assessed when
using efficacious vaccination schedules, as well as the environmental,
biosecurity, management and control of replacement gilts.